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The discovery of the pulmonary circulation was reported in the 13th century by Ibn al-Nafis (1213–1288) in the “Commentary on Anatomy in Avicenna’s Canon” and, probably independently, in the 16th century by Michael Servetus (1511–1553) in the “The Restoration of Christianity.”1 The pulmonary circulation as a separate high-flow low-pressure system is the end result of an evolutionary process aimed at the optimization of gas exchange of endothermic birds and mammals.2 Evolution from ancestors of fishes to amphibians, reptiles, and finally birds and mammals has led to progressively greater oxygen consumption requiring thinner pulmonary blood gas barrier. The alveolo-capillary membrane in mammals is a vulnerable structure only 0.3 µm thick. Preservation of the integrity of this barrier requires complete separation of the pulmonary circulation from the systemic circulatory systems, which is accompanied by a progressive unloading and reshaping of the right ventricle as a thin-walled flow generator.
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The extreme possible physiologic stresses on the pulmonary circulation are exercise and hypoxia. Exercise increases oxygen uptake and carbon dioxide output up to some 20-fold above resting values and increases cardiac output up to some 6-fold. Strenuous exercise may eventually alter gas exchange because of excessive capillary filtration and stress failure, or expose the right ventricle to excessive loading resulting in a limitation of maximum cardiac output. Hypoxia adds the burden of further increase in pulmonary vascular pressures due to hypoxic pulmonary vasoconstriction.
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PULMONARY VASCULAR PRESSURES AND RESISTANCE
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Pulmonary blood flow is determined by the driving pressure in the pulmonary circulation and resistance to flow, as discussed below.
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Pulmonary blood flow (CO) is driven by a pressure difference between an inflow pressure, or mean pulmonary artery pressure (mPAP), and an outflow pressure, or mean left atrial pressure (LAP). From these measurements, resistance to flow in the pulmonary circulation can be approximated by a single number, pulmonary vascular resistance (PVR), which depends on the ratio between (mPAP - LAP) and CO:
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In clinical practice, measurements of pulmonary vascular pressures and pulmonary blood flow are performed during a catheterization of the right heart with triple-lumen, fluid-filled balloon- and thermistor-tipped catheter technology introduced by Swan, Ganz, and Forrester in the 1970s.3,4
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As illustrated in Fig. 13-1, the procedure allows for the estimation of LAP from a balloon-occluded or wedged PAP (PAOP or PAWP). Wedged or occluded PAP are usually grouped under the term PAWP, as a discrepancy may occur only in case of an increase in large pulmonary vein resistance, which is very rare. The fractal structure of the pulmonary arterial and venous trees allows for a stop-flow phenomenon downstream of occlusion and de facto extension of the fluid-filled lumen of the catheter to same diameter pulmonary veins. A left heart catheterization allows for the measurement of left ...